Rhythmic contractions of a healthy heart are normally controlled by the sinoatrial (SA) node, specialized cells located in the superior right atrium. The SA node is the normal pacemaker of the heart, typically initiating 60–100 heart beats per minute. When the SA node is pacing the heart normally, the heart is said to be in normal sinus rhythm (NSR).
A heart rhythm that deviates from normal sinus rhythm is an arrhythmia. Arrhythmia is a general term used to describe heart rhythm disturbances arising from a variety of physical conditions and disease processes. Bradycardia occurs when the heart rhythm is too slow and has a number of etiological sources including tissue damage due to myocardial infarction, exposure to toxins, electrolyte disorders, infection, drug effects, hypoglycemia or hypothyroidism. Bradycardia also may be caused by sick sinus syndrome, wherein the SA node loses its ability to generate or transmit an action potential to the atria.
Supraventricular arrhythmias originate in the atria or surrounding tissues (vena cavae, pulmonary veins, etc.) resulting in a rapid atrial rate. One mechanism for supraventricular tachycardia is an accessory pathway between the ventricular and atrial tissue. The accessory pathway, in combination with the normal AV nodal pathway, forms a conducting loop that can support reentry. The reentrant wave circulates through the pathway and elevates the heart rate. Atrial flutter is another type of supraventricular arrhythmia and arises when an electrical wavefront circulates around an anatomical or functional obstacle in the atrial myocardium. Atrial fibrillation occurs when electrical impulses initiate in the atria at irregular intervals and usually at a rate of greater than 300 impulses per minute. As a result, impulses reaching the AV node, and thus the ventricles, are also irregular, causing irregular contractions of the ventricles at an increased rate.
Ventricular tachycardia occurs when impulses are initiated in the ventricular myocardium with a rate more rapid than the intrinsic rate of the SA node. Ventricular tachycardia (VT) is characterized by a rapid heart beat and typically results from damage to the ventricular myocardium from a myocardial infarction. Ventricular tachycardia can quickly degenerate into ventricular fibrillation (VF). Ventricular fibrillation is a condition denoted by extremely rapid, uncoordinated contractions of the ventricles. The rapid and erratic contractions of the ventricles degrades the ability of the ventricles to effectively pump blood to the body and the condition is fatal unless the heart is returned to sinus rhythm within a few minutes.
Implantable cardiac rhythm management (CRM) devices may incorporate both defibrillation and pacemaker circuitry used to treat patients with serious arrhythmias. CRM devices typically include circuitry to sense signals from the heart and a pulse generator for providing electrical stimulation to the heart. Leads extending into the patient's heart are connected to electrodes that contact the myocardium for sensing the heart's electrical signals and for delivering stimulation to the heart in accordance with various therapies for treating the arrhythmias described above.
Pacemakers deliver low energy electrical pace pulses timed to assist the heart in producing a contractile rhythm that maintains cardiac pumping efficiency. Pace pulses may be intermittent or continuous, depending on the needs of the patient. Defibrillators apply one or more high energy pulses to the heart to terminate a tachyarrhythmia by shocking the heart into a normal rhythm.
There exist a number of categories of pacemaker devices, with various modes for sensing and pacing the heart. Single chamber pacemakers pace and sense one heart chamber. Dual chamber pacemakers may pace and sense two chambers of the heart. Standard dual chamber pacemakers include electrodes positioned in the right atrium and right ventricle to provide atrial and ventricular pacing. In cardiac resynchronization devices, a multichamber pacemaker may include electrodes positioned to contact cardiac tissue within or adjacent to both the left and the right ventricles for pacing both the left and right ventricles. This type of device allows bi-ventricular pacing therapy to be applied, for example, to coordinate ventricular contractions when a patient suffers from congestive heart failure (CHF). Furthermore, a pacemaker may include electrodes positioned to contact tissue within or adjacent to both the left and the right atria to enable bi-atrial pacing. Bi-atrial pacing therapy may be used, for example, to control atrial tachyarrhythmias. Future devices may pace different combinations of the four chambers or even multiple sites within the same chamber to achieve optimal coordination of contraction, arrhythmia suppression, or control of cardiac remodeling.
When a pace pulse produces a contractile response in a heart, the contractile response is typically referred to as capture, and the electrical waveform corresponding to capture is denoted an evoked response. A pace pulse must exceed a minimum energy value, denoted the capture threshold, to produce a contraction. Pacing therapy applied to multiple sites on the heart, such as the bi-ventricular or bi-atrial pacing therapies discussed above, produces a change in the temporal contraction pattern. When a pacing pulse is closely coupled to intrinsic cardiac electrical activity, the result is fusion. The evoked response from fusion beats may be confused with either capture or noncapture depending on the coupling interval between the intrinsic and paced electrical waveforms. It is desirable for a pace pulse to have sufficient energy to produce a contractile response in the heart chambers stimulated without expending energy in excess of the capture threshold. Accurate detection of the capture threshold is required for efficient pace energy management. If the pace pulse energy is too low, the pace pulses may not reliably produce a contractile response in the heart resulting in ineffective pacing. If the pace pulse energy is too high, the result may be patient discomfort as well as shorter battery life.
Capture detection, including fusion management, allows the cardiac rhythm management system to verify whether capture occurs in the stimulated heart chamber or chambers following a pacing pulse. In particular, capture detection for multiple heart chambers may be used in conjunction with bi-ventricular, bi-atrial pacing, or multisite pacing therapies. If loss of capture is detected, the cardiac rhythm management system may deliver a back-up pulse at a higher energy level to ensure capture and subsequently initiate a threshold test to reset the pacing output to a safe level.